PUBLICATION
Crosstalk of oxidative damage, apoptosis, and autophagy under endoplasmic reticulum (ER) stress involved in thifluzamide-induced liver damage in zebrafish (Danio rerio)
- Authors
- Yang, Y., Dong, F., Liu, X., Xu, J., Wu, X., Liu, W., Zheng, Y.
- ID
- ZDB-PUB-181110-3
- Date
- 2018
- Source
- Environmental pollution (Barking, Essex : 1987) 243: 1904-1911 (Journal)
- Registered Authors
- Keywords
- Autophagy, ER, Oxidative damage, Thifluzamide, Zebrafish
- MeSH Terms
-
- Anilides/toxicity*
- Animals
- Antioxidants/metabolism
- Apoptosis/drug effects*
- Autophagy/drug effects*
- Chemical and Drug Induced Liver Injury
- Endoplasmic Reticulum Stress/drug effects*
- Liver/drug effects*
- Malondialdehyde/metabolism
- Oxidative Stress/drug effects*
- Thiazoles/toxicity*
- Water Pollutants, Chemical/toxicity
- Zebrafish/metabolism
- Zebrafish/physiology*
- PubMed
- 30408879 Full text @ Environ. Pollut.
Citation
Yang, Y., Dong, F., Liu, X., Xu, J., Wu, X., Liu, W., Zheng, Y. (2018) Crosstalk of oxidative damage, apoptosis, and autophagy under endoplasmic reticulum (ER) stress involved in thifluzamide-induced liver damage in zebrafish (Danio rerio). Environmental pollution (Barking, Essex : 1987). 243:1904-1911.
Abstract
Although the hepatotoxicity of thifluzamide in zebrafish has been characterized, its toxic mechanisms have not been fully explored. The present study demonstrated that thifluzamide damaged the zebrafish liver and endoplasmic reticulum (ER). In addition, thifluzamide significantly changed the expression of genes encoding antioxidant proteins and increased the malondialdehyde (MDA) content, leading to oxidative damage in zebrafish liver. Additionally, the autophagic ultrastructure was observed by transmission electron microscopy (TEM), and LC3-I/LC3-II conversion was obviously upregulated under western blotting (WB) measurements, verifying that autophagy was induced by thifluzamide. Moreover, the activities of Caspase-3 and Caspase-9 were obviously decreased, indicating that apoptosis was inhibited in adult zebrafish exposed to a higher concentration of thifluzamide. In summary, oxidative damage and autophagy but not apoptosis under ER injury might lead to the hepatotoxicity of thifluzamide in zebrafish. Our findings provide a new mechanistic insight into the toxicity of thifluzamide in zebrafish.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping